gout(redirected from Uric acid crystal deposition in joint)
Also found in: Dictionary, Thesaurus, Medical, Legal.
gout,condition that manifests itself as recurrent attacks of acute arthritis, which may become chronic and deforming. It results from deposits of uric aciduric acid
, white, odorless, tasteless crystalline substance formed as a result of purine degradation in man, other primates, dalmatians, birds, snakes, and lizards. The last three groups of animals also channel all amino acid degradation into the formation of glycine, aspartic
..... Click the link for more information. crystals in connective tissue or joints. The presence of increased uric acid (a breakdown product of DNA) in the body distinguishes gout from other forms of arthritisarthritis,
painful inflammation of a joint or joints of the body, usually producing heat and redness. There are many kinds of arthritis. In its various forms, arthritis disables more people than any other chronic disorder.
..... Click the link for more information. , although hyperuricemia alone, which often occurs in the complete absence of gout, is not thought to be the sole causative factor. About 95% of patients with this disorder are men, usually over 30. Gout is associated with obesity and a hereditary factor in some cases. Diet also has an affect on gout. Consumption of meat and seafood, which are high in purine (from which digestion produces uric acid), increase the risk of gout, and gout is worsened by kidney problems and drinking alcoholic beverages, which slow the excretion of uric acid. Beer, which is higher than other alcoholic beverages in purines, also has been shown to increase the risk of gout.
Gout usually begins with an acute attack of pain, inflammation, extreme tenderness, and redness in the affected joint—often the big toe and sometimes the ankle or knee. After repeated attacks the disease can cause the deposition of sodium urate crystals in the tissues about the joints, causing stiffness and deformity. The aim of treatment is to minimize the formation of uric acid crystals. A high liquid intake that increases daily urine output is usually recommended. An acute attack of gout is usually treated with nonsteroidal anti-inflammatory drugs, such as indomethecine or naproxen, or the corticosteroid prednisone. Colchicine, a preparation of the meadow saffronmeadow saffron
or autumn crocus,
perennial garden ornamental (Colchicum autumnale) of the family Liliaceae (lily family). Native to Europe and N Africa, it has escaped from gardens to meadows and fields in some parts of the United States.
..... Click the link for more information. , used since 1763 for gout, is still used when symptoms are not controlled by other drugs. Allopurinol and other xanthine oxidase inhibitors are used to prevent gout attacks in patients with chronically elevated uric acid levels; they lower uric acid concentrations in the blood by inhibiting the conversion of xanthine to uric acid.
a disease caused by a disturbance of purine metabolism and by deposits of urates in the tissues, affecting mainly the joints and kidneys.
Gout constitutes 2.5 percent of all cases of joint diseases. Primary gout results from diet or from congenital metabolic disorders that cause such forms of the disease as familial gout. Secondary gout, which is less common, is caused by lead poisoning, by some diseases of the blood, and, less commonly, by other factors.
Gout chiefly affects middle-aged men. It is chronic or occurs in the form of acute recurrent attacks. An attack of gouty arthritis is marked by sudden pain, generally in the big toe. The pain rapidly intensifies and is accompanied by swelling and reddening. An attack can be provoked by trauma, excessive cold, or ingestion of alcohol or of food rich in purine bases and lasts from several hours to several days. After an attack, the pain subsides and the functions of the joint are restored. However, each new attack is longer and more intense. In most cases, gout gradually becomes chronic. Owing to the increased uric-acid concentration in the blood serum, urates are deposited in the tissues, generally near the external concha auriculae and around the joints, whose movements as a result become limited. The kidneys are frequently affected.
Gout is diagnosed on the basis of the following symptoms: acute attacks of painful swelling of a single joint, generally the big toe; deposits of urates (tophi); elevated uric-acid levels in the blood serum; the presence of uric-acid crystals in the synovia or synovial fluid; and characteristic changes in roentgenograms of joints.
Acute attacks of gout are treated with bed rest, colchicine, Rheopyrine, Ketazon, Indacin, or other agents capable of arresting the attacks. Chronic forms of the disease are treated with sodium carbonate, Anturane, Benemid, allopurinol, and other drugs that prevent the formation of uric acid or accelerate its excretion from the body. Drinking of copious fluids is recommended, and a diet low in calories and purines is prescribed. Consumption of alcohol, meat broths, liver, and kidneys is prohibited. Eggs and cheese are permitted in limited amounts, and fruit and groats are allowed. A stay at a health resort is recommended if the kidneys are not involved.
REFERENCEPikhlak, E. G. Podagra. Moscow, 1970.
V. M. CHEPOI